Abstract
We report the molecular investigations of a large influenza A(H3N2) outbreak, in a season characterised by sharp increase in influenza admissions since December 2016. Analysis of haemagglutinin (HA) sequences demonstrated co-circulation of multiple clades (3C.3a, 3C.2a and 3C.2a1). Most variants fell into a novel subclade (proposed as 3C.2a2); they possessed four unique amino acid substitutions in the HA protein and loss of a potential glycosylation site. These changes potentially modify the H3N2 strain antigenicity.
Highlights
An outbreak of influenza A(H3N2) was first notified in our London centre on 30 December 2016
The outbreak coincided with unusually high ongoing circulation of respiratory syncytial virus (RSV) (Figure 1), and affected both patients and staff in the acute medical unit (AMU)
We suspected that the sharp increase in the number of influenza A(H3N2) infections may have been caused by the emergence of a new genetic variant of H3N2, a hypothesis investigated through generation sequencing (NGS) of influenza A(H3N2) strains
Summary
Emergence of a novel subclade of influenza A(H3N2) virus in London, December 2016 to January 2017. Most variants fell into a novel subclade (proposed as 3C.2a2); they possessed four unique amino acid substitutions in the HA protein and loss of a potential glycosylation site. These changes potentially modify the H3N2 strain antigenicity. We suspected that the sharp increase in the number of influenza A(H3N2) infections may have been caused by the emergence of a new genetic variant of H3N2, a hypothesis investigated through generation sequencing (NGS) of influenza A(H3N2) strains
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